Expression of functions by normal sheep alveolar macrophages and their alteration by interaction with Mycoplasma ovipneumoniae.
Normal sheep alveolar macrophages collected by bronchial lavage were exposed to live or heat-killed Mycoplasma ovipneumoniae organisms, and their capability to ingest Staphylococcus aureus and to elicit antibody-dependent cellular cytotoxicity against sensitized chicken red blood cells was tested. Controls consisted of non-infected macrophages in M199 medium. In addition, the effect of M. ovipneumoniae on expression of surface molecules on these sheep alveolar macrophages was determined. The percentage of S. aureus ingested by nontreated sheep alveolar macrophages was significantly higher than that of infected macrophages. Live mycoplasmas were more effective in suppressing the ingestion of S. aureus by these macrophages than killed mycoplasmas. Both live and killed mycoplasmas suppressed the cytolytic effect of the sheep alveolar macrophages to a similar degree. About 78% and 45% of the normal sheep alveolar macrophages had IgG and complement receptors, respectively. Infection of these macrophages with M. ovipneumoniae decreased significantly the expression of IgG receptors but had no effects on complement receptors. There were substantial increases in the expression of both MHC class I and class II by the mycoplasma-induced macrophages as compared with unstimulated macrophages. Live mycoplasmas were more effective in inducing expression of both classes than killed mycoplasmas. The results, taken together, suggest that M. ovipneumoniae induced alterations in macrophage activities and this may be a contributing factor in the pathogenesis of respiratory disease induced by the organism.
Niang
M
M
Department of Microbiology, Immunology and Preventive Medicine, College of Veterinary Medicine, Iowa State University, Ames 50011, USA.
Rosenbusch
R F
RF
Lopez-Virella
J
J
Kaeberle
M L
ML
D000818:Animals; D000920:Antibody-Dependent Cell Cytotoxicity; D003601:Cytotoxicity Tests, Immunologic / Q000662:veterinary; D015395:Histocompatibility Antigens Class I / Q000096:biosynthesis; D000949:Histocompatibility Antigens Class II / Q000096:biosynthesis; D016676:Macrophages, Alveolar / Q000276:immunology* / Q000382:microbiology / Q000473:pathology; D009174:Mycoplasma / Q000276:immunology* / Q000472:pathogenicity; D011951:Receptors, Complement / Q000032:analysis; D017452:Receptors, IgG / Q000032:analysis; D012397:Rosette Formation; D012756:Sheep / Q000276:immunology*; D013203:Staphylococcal Infections / Q000276:immunology / Q000382:microbiology / Q000662:veterinary; D013211:Staphylococcus aureus / Q000276:immunology
D015395:Histocompatibility Antigens Class I; D000949:Histocompatibility Antigens Class II; D011951:Receptors, Complement; D017452:Receptors, IgG